CHF is associated with CSR, characterized by a crescendo-decrescendo breathing pattern with central apnea or hypopnea occurring at the nadir of ventilatory drive. The prevalence of sleep apnea in patients with CHF is about 50% (30,39-41). In one prospective study, Javeheri et al. demonstrated that 51% of male patients with CHF had sleep-disordered breathing, 40% had CSA, and 11% had obstructive apnea. In another study, Sin et al. (35) identified CHF patients at high risk for the presence of sleep apnea in 450 consecutive patients with CHF who underwent polysomnography. Using an apnea-hypopnea index cutoff of 10 per hour of sleep, 302 patients had sleep-disordered breathing (66%). Risk factors for CSA were male gender, atrial fibrillation, age > 60 years, and daytime hypocapnia (Pco2 < 38 mmHg). In contrast, risk factors for OSA differed by gender. Body mass index was the only independent determinant in men; age more than 60 years was the only independent determinant for women. Overall, there was a near-equal distribution between OSA and CSA. Thus, central apnea is common in patients with CHF; patients at high risk can be identified by history, electrocardiography, and arterial blood gases.
The precise mechanism(s) of central apnea in patients with CHF remain incompletely understood. The initial apnea is likely related to pulmonary congestion (30) leading to hyperventilation and hypocapnia. Thus, the initial central apnea may develop even after modest hyperpnea, owing to the precarious proximity of PaCO2 to the apneic threshold. Xie et al. studied 19 stable patients with CHF with (12 patients) or without (7 patients) CSA during NREM sleep. Patients with central apnea showed no rise in PETCO2 from wakefulness to sleep; eupneic PETCO2 was closer to the apneic threshold than patients without central apnea as shown in Figure 2. The narrowed delta PETCO2 predisposes the patient to the development of apnea and subsequent breathing instability.
The aforementioned mechanisms account for the occurrence of central apnea. However, the mechanism(s) of sustained breathing instability and periodic breathing is not clear. There is conflicting evidence regarding the role of prolonged circulatory delay in the genesis of periodic breathing in patients with heart failure (42-45).
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